Filtyp
Antiviral Action against Type 1-diabetes Autoimmunity I AVAnT1A undersöks om utvecklingen av diabetesspecifika autoantikroppar kan förhindras eller fördröjas hos barn med förhöjd risk för sjukdomen genom vaccination mot SARS-CoV-2 (COVID-19) vid 6 månaders ålder. Studien har också ett bredare mål, nämligen att studera vilka infektioner små barn drabbas av och om det finns ett samband mellan dessa
https://www.gppad.lu.se/vara-studier/avant1a - 2026-07-05
En studie för uppföljning av barn med antingen förhöjd genetisk risk för typ 1-diabetes eller barn med diabetesspecifika autoantikroppar IT1D är en studie man kan delta i om man avböjt att delta i en preventionsstudie eller om man avslutat en tidigare studie tex. POInT. Om man har fått reda på att man har diabetesspecifika autoantikroppar på något annat vis tex. via en annan studie kan man också d
https://www.gppad.lu.se/vara-studier/it1d - 2026-07-05
Intensive Dietary & Activity Counselling I IDAC undersöks om intensiv (mer regelbunden) kost-och fysisk aktivitetsrådgivning under de två första levnadsåren minskar frekvensen av typ 1-diabetesrelaterade autoantikroppar och om det påverkar barnets insulinproducerande celler. Ett annat mål är att studera om en intensiv kost-och fysisk aktivitetsrådgivning kan påverka barnets tillväxt. En teori är a
https://www.gppad.lu.se/vara-studier/idac - 2026-07-05
Den första interventionsstudien inom GPPAD, POInT, startade 2018. Sedan dess har många barn varit med i någon av GPPADs studier. Det finns än så länge en unik familj i GPPAD i Sverige som har ett barn i varje GPAPD studie, ett i POInT, ett i SINT1A och nu även ett i AVAnT1A. Vid lillasyster Albas första besök i AVAnT1A passade jag på att ställa några frågor till mamma Rebecca eftersom hon, om någo
https://www.gppad.lu.se/en-trippel-i-gppad - 2026-07-05
Primär oral insulinterapi (Primary Oral Insulin Trial) POInT-studien är avslutad och deltagarna har nu fått reda på om de har fått placebo eller oralt insulin samt vilken effekt det har haft. I POInT, som startade 2017, undersöktes om utvecklingen av typ 1-diabetes kunde förhindras hos barn med förhöjd genetisk risk för sjukdomen genom förebyggande behandling med oralt insulin (via munnen).I studi
https://www.gppad.lu.se/vara-studier/avslutade-studier/point-0 - 2026-07-05
POInT-studien är en primär preventionsstudie där barn från 4–7 månaders ålder får oralt Insulin eller overksamt pulver varje dag fram till 3 års ålder. Barnen som deltar har förhöjd ärftlig risk att utveckla autoantikroppar mot betacellerna i bukspottskörteln, som tillverkar insulin. Studien inkluderade 1050 barn i Tyskland, Sverige, England, Polen och Belgien. Syftet med behandlingen var att ins
https://www.gppad.lu.se/forskningsresultat-och-media/resultat-fran-point-studien-primary-oral-insulin-therapy - 2026-07-05
In June 2022, Sofia Bergh started her PhD studies in TNU supervised by Prof. Åsa Petersén. The overall aim of the PhD project is to investigate the cellular and molecular mechanisms of limbic system pathology of Huntington’s disease. Her first original research article is in press titled “Effects of mutant huntingtin in oxytocin neurons on non-motor features of Huntington’s disease” in Neuropathol
https://www.huntington-research.lu.se/team/sofia-bergh-phd-student - 2026-07-05
Weydt P, Dupuis L and Petersen Å. Handbook of Clinical Neurology 157: 761-775 (2018) Abstract Huntington disease (HD) is a paradigmatic autosomal-dominant adult-onset neurodegenerative disease. Since the identification of an abnormal expansion of a trinucleotide repeat tract in the huntingtin gene as the underlying genetic defect, a broad range of transgenic animal models of the disease has become
https://www.huntington-research.lu.se/thermoregulatory-disorders-huntington-disease - 2026-07-05
Baldo B, Soylu R and Petersén ÅPLoS One 8(12) (2013)AbstractHuntington's disease (HD) is a fatal neurodegenerative disorder caused by an expanded polyglutamine repeat in the huntingtin protein. Neuropathology in the basal ganglia and in the cerebral cortex has been linked to the motor and cognitive symptoms whereas recent work has suggested that the hypothalamus might be involved in the metabolic
Bergh S, Gabery S, Tonetto S, Kirik D, Petersén Å and Cheong RY. Neuropathology and Applied Neurobiology. 2023;49(2):e12891. doi:10.1111/nan.12891 [published correction appears in Neuropathol Appl Neurobiol. 2023 Jun;49(3):e12905]. Abstract Background: Early non-motor features including anxiety, depression and altered social cognition are present in Huntington's disease (HD). The underlying neurob
In May 2022, Karin Dalene Skarping started her PhD studies in TNU supervised by Prof. Åsa Petersén. The overall aim of the PhD project is to study genetic mechanisms that may modify the disease course and pathology of Huntington disease. One of her current research projects is aimed to examine associations between germline pathogenic variants in mismatch-repair (MMR) genes and CAG-repeats in HTT,
https://www.huntington-research.lu.se/team/karin-dalene-skarping-phd-student - 2026-07-05
Sofia Hult Lundh1, Nathalie Nilsson1, Rana Soylu1, Deniz Kirik2 and Åsa Petersén1.1Translational Neuroendocrine Research Unit, Department of Experimental Medical Science, Lund University, Lund SE-221 84, Sweden.2Brain Repair and Imaging in Neural Systems (BRAINS) Unit, Department of Experimental Medical Science, Lund University, Lund SE-221 84, Sweden.Human Molecular Genetics 22: 3485-3497 (2013)A
Linda Holmquist Mengelbier is a paediatric cancer researcher who now, in parallel to her cancer effort, has started to work with the neurodegenerative disorders Huntington disease and ALS. Her focus in the cancer field has been on the embryonal pediatric solid tumors neuroblastoma and Wilms tumor. Neuroblastoma is a sympathetic nervous system tumor derived from the neural crest, whereas Wilms tumo
https://www.huntington-research.lu.se/team/linda-holmquist-mengelbier-phd - 2026-07-05
Soylu-Kucharz R, Adlesic N, Davidsson M, Björklund T, Björkqvist M and Petersén Å. bioRxiv 2023.03.04.530949; First published March 4, 2023, https://doi.org/10.1101/2023.03.04.530949 Abstract Huntington’s disease is a fatal neurodegenerative disorder caused by an expanded CAG triplet repeat in the huntingtin (HTT) gene. Previous research focused on neuropathology in the striatum and its associatio
Dalene Skarping K, Arning L, Petersén Å, Nguyen HP and Gebre-Medhin S.Sci Rep. 2024;14(1):4300. Published 2024 Feb 21. doi:10.1038/s41598-024-54277-5AbstractDNA mismatch repair (MMR) is thought to contribute to the onset and progression of Huntington disease (HD) by promoting somatic expansion of the pathogenic CAG nucleotide repeat in the huntingtin gene (HTT). Here we have studied constitutional
Lilja Andersson P, Juth N, Petersén Å, Graff C and Edberg AE.Lund University, Sweden.Nursing Ethics 20: 189-199 (2013)AbstractThe aim of this study was to describe the experiences of undergoing a presymptomatic genetic test for the hereditary and fatal Huntington’s disease, using a case study approach. The study was based on 18 interviews with a young woman and her husband from the decision to und
https://www.huntington-research.lu.se/ethical-aspects-undergoing-predictive-genetic-testing-huntingtons-disease - 2026-07-05
In 2024, Jennifer moved from Sydney, Australia to Lund, Sweden to start her PhD studies at the TNU, supervised by Pof. Åsa Petersén. In utilizing novel AAV-vectors and crossbreeding of animal models, Jennifer’s project aims to elucidate the specific hypothalamic circuitries important for the control of metabolism and emotion, with relevance to Huntington’s Disease, Amyotrophic Lateral Sclerosis an
https://www.huntington-research.lu.se/team/jennifer-oraha-phd-student - 2026-07-05
Lundh SH, Soylu R and Petersén Å.Translational Neuroendocrine Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.PLoS ONE 7(12): e51168 (2012).AbstractMetabolic and psychiatric disturbances occur early on in the clinical manifestation of Huntington’s disease (HD), a neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin (HTT) gene. Hypot
Hagen N, Lundin S, O'Dell T and Petersén Å.Culture Unbound 4: 537-557 (2012)AbstractModernity has meant a cultural and social differentiation within the western socie- ty, which, according to Jürgen Habermas’ theory on communication, can be seen as a division between different forms of actions that takes place in different realms of the society. By combining Habermas’ notions of lifeworld and sys
https://www.huntington-research.lu.se/better-or-worse-lifeworld-system-and-family-caregiving-chronic-genetic-disease - 2026-07-05
Bergh S, Casadei N, Gabery S, Simonsson O, Duarte JMN, Kirik D, Nguyen HP and Petersén Å.Acta Neuropathologica Communications. 2025;13(1):119. Published 2025 May 27. doi:10.1186/s40478-025-02018-8AbstractTAR DNA-binding protein 43 (TDP-43) pathology is linked to the neurodegenerative disorders amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Huntington disease (HD). Dysregul
